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Isolated perfused Langendorff rat 
hearts were used for comparing effects of the
 calcium antagonist verapamil on the following 
two models of heart injury: local ischemia (ligature of the anterior interventricular artery) and
 general hypoxia (perfusate saturated with nitrogen). The degree and extent of injury were
 assessed by measuring the activity of lactate 
dehydrogenase in venous effluents from the 
heart, contractility, heart rate, coronary flow,
and ECG. Lactate dehydrogenase activity in the
 venous effluents was the marker of cellular 
injury. Verapamil had a beneficial effect on the 
contractility and rhythmicity after reoxygenation 
of the hypoxically injured heart. Verapamil significantly reduced the release of lactate dehydrogenase during reperfusion and reoxygenation of ischemic and hypoxic hearts, respectively. Maximal lactate dehydrogenase activities 
during reperfusion of the ischemic hearts, treated with verapamil, were 6.3 ±1.9 kat/g x 
ml/min, compared to activities obtained from
 untreated ischemic hearts, 23.6 ± 5.4 kat/g x
 ml/min. Maximal lactate dehydrogenase activities during reoxygenation of the hypoxic hearts, treated with verapamil, were 3.6 ± 0.9 kat/g x
ml/min, compared to the activities of untreated 
hypoxic hearts, 8.0 ± 2.4 kat/g x ml/min. Results of our experiment showed cytoprotective 
effects of verapamil, especially on local ischemic injury of the isolated heart.